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Immune System 1.Cellular Elements T Lymph. Helper,suppressor,cytotoxic ,killer 2.Humoral Elements Antibodies,complements,cytokines,other circulating p.p Functions Appropriate Monitor+defense Inappropriate Hypersensetive allergic reactions Allergic Reactions Type I Immediate A/IgE-mast+basophils anaphylaxis,all.rhinitis ,ext.asth. Type II Cytotoxic IgG or IgM/Antigens on the surface of foreign cells ABO-incompatiblity,drug induced hemolytic,heparin/thrombo. Type III Immune Complex Insoluble Ant/Ab deposit in the microvasculature Ca /neutrophils---tissue damage Type IV Delayed Antigen/T-cells—lyphocyte regulation,Macrophage activation+Mononuclear cell infiltration contact dermatitis,graft rejection Definitions • Anaphylasis:life-threatening allergic reactions mediated by • • • • • antibodies Anaphylactoid:life-threatening allergic reaction Not mediated by antibodies (unable to prove antibody involvement). Antigen:Molecules capable of stimulating an immune response(AB or Lymphocyte). Heptan:small molecule bind to P.P to form macromolecule. Antibodies:immunoglobulins that can recognize and bind to a specific antigen.IgG,IgA,IgM,IgD+IgE Complement:20 different protiens that bind to activated antibodies,other complement protiens and cell membranes. Series of inhibitors regulates activation(C1 esterase inhibitor deficiency) Angoneurotic Edema • Painless,Nonpitting,Nonpuritic,Demarcated edema of deep dermis and Sc.,usually involving face, airway,GIT and extremities. • Types:Hereditary deficiency or dysfunction of C1 esterase inhibitor (less than 50% of normal C1 esterase is produced). Acquired,cosumtion or autoantibodies • ACEI-blocks metabolism of bradykinin and substance P . • Codeine, generation of tissue bradykinin from mast cells degranulation. Clinical Presentation HAE:1:50,000-1:150,000 Age: by 30yr,98% of patients have S/S. Triggering factors: minor or even trivial trauma or emotional upset. AAE:less than HAE. Age: older age ,associated with malignance. 96% had swelling of extremities. 93% had recurrent abdominal pain. 85% had edema of the face. 64% had oropharyngeal involvement. 14-33% may die from laryngeal edema. Urticaria(erythematous ,pruritic,cutaneous elevationsof the skin that blanch with pressure)can occur in some patients. Drug therapies for C1 INH Deficiency 1. Antifibrinolytic:EACA,tranexamic acid.Inhibit 2. 3. 4. plasminogen and plasmin activity,limiting the formation of plasmin,which can activate C1.Ache,fatigue,hypotenion,+TE. Androgen,increasesC1 INH by the liver. Weight gain,headch,myalgia,so on. FFP:contains C1 INH,but also contains kinins and C2,C4 that may fuel complement activation. Purified C1 INH concentrate, partial resolution of symptoms within 1 h.,complete resolution within 24 h.can increaseC1 INH by 50% over 15 min. pooled plasma. Treatment of Acute Attack 1.Stop administration of suspected antigen. 2.Maintain airway with 100% oxygen. 3.I.V crystalloid/colloid. 4.Epinephrine(5-10ug.i.v,titrate as needed), Secondary treatment: 1.Diphenhyramine(.5-1mg./kg.). 2.Catecholamine infusions(Ep.4-8ug/min.,Norep.48ug./min.,iosproterenol.5-1ug./min). 3.Aminophylline(5-6mg./kg.over20min.inf. .9-1mg/kg/h). 4.Corticosteroids(.1-1g.hydrocortisone,1-2g.methyprednisolone). 5.NaHCO3,.5-1mEq/kg.with persistent hypotension or acidosis. 6.Airway evaluation ( prior to extubation). Catecholamines • Epinephrine • Alpha-adrenergic--VC . • B2 st.--bronchodilation+inhibits mast cells ,basophils mediator • • • • • • • • • • release by increasing cAMP. Rout of administeration,dose depend on the patient's condition. Racemic Epi.(sour white crystalline,D+L tartaric acid). Dose:2.25% Nebulize mixure. Child under 6 month --0.25ml. Child above 6 month--0.5 ml. Adolescent 0.75 ml. Adult 1 ml. Add 2-3.5 ml. Onset 5-10 min.,last 90-120 min. May be repeated in 30 min. Norepinephrine • May be used in refractory hypotension. • 0.05-0.1 ug/kg/min.(4-8 ug/min.) Isoproterenol • May be use in refractory bronchospasm,pulmonary • • hypertension, or Rt.ventriculer dysfunction. 0. 01-0.02 ug./kg./min.(0.5-1ug/min.) Profound B2adrenergic effects-systemic VD. Aminophylline • Nonspecific phosphodiesterase inhibitor-bronchodilator. • Decrease pulmonary vascular resistance. • Improve Rt and Lf ventricular contractility. • Decrease histamine release from mast, and basophilic cells •Corticosteroids • Decrease arachidonic acid metabolites by inhibiting phospholipids membrane breakdown. • May alter the activation and migration of other inflammatory cells • May require hours to work, but they still in practice in refractory bronchospasm or shock. • Hydrocortisone is recommended in IgEmediated reaction • 0.25-1 g. • Methylprednisolone is recommended for complement mediated reaction,(30-35mg/kg) Special Anesthetic Consideration Avoid airway manipulation as much as possible( regional or mask inhalation). LMA,it is reasonable to assume that its large surface contact area may lead to worsened airway edema. Fiberoptic intubation,in presence of severe airway swelling and the demand for acute intervention can greatly limit the effectiveness of FO intubation. When performing emergency laryngoscopy and intubation,the attendance of an otolaryngologist is mandatory should a tracheostomy be necessary OR, is the best place for airway instrumentation, this may not always possible. Nonimmunologic Release of Histamine • The mechanisms appear to be noncytotoxic degranulation of mast cells, but not basophils. • Cutaneous mast cells are the only cell population that release histamine in response to drugs or endogenous neuropeptides. Allergic Drug Reactions • 5% of adult in US may be allergic to one or more • • • drugs. 15% of adult in US believe ,they are allergic to specific medication. They refer to adverse drug effects as being allergic in nature. A drug may produce different reactions in different patients or spectrum of reactions in the same patient. A drug can produce anaphylaxis (Type I). Hemolysis (type II). Serum sickness (type III). Contact dermatitis (type IV).